Current methods for treating sporadic Alzheimer's mainly target amyloid beta and tau but overlook the critical issue of calcium dysregulation, which is significant in the disease's earlier stages.
The study explores the effects of a GCPII inhibitor, 2-MPPA, on aged macaques to see if it can enhance calcium signaling and reduce tau hyperphosphorylation.
Results indicated that 2-MPPA treatment led to lower levels of tau pathology and correlated with cognitive improvements, suggesting that targeting GCPII may be a promising strategy for addressing Alzheimer's-related inflammation.*